Anthrax is a potentially lethal human infection. The pathogen responsible for anthrax is the Gram-positive rod-shaped bacterium, Bacillus anthracis (B. anthracis). In many situations, the body protects against pathogenic infections by producing antibodies that bind to antigens on the pathogen to facilitate the removal or “clearance” of the pathogens by a process called phagocytosis, wherein phagocytic cells (for example neutrophils and macrophages) identify, engulf, and subsequently destroy the pathogens. However, some pathogens, such as B. anthracis, avoid phagocytosis by encapsulating themselves with a capsule that is poorly immunogenic and has antiphagocytic properties.
The virulence of B. anthracis is dependent on anthrax toxin (AT) and the poly-γ-D-glutamic acid (γDPGA) capsule. γDPGA is poorly immunogenic and does not induce booster responses. In addition, the γDPGA capsule shields the vegetative form of B. anthracis from agglutination by monoclonal antibodies to its cell wall polysaccharide. Thus, few effective antibody therapies directed against B. anthracis have been developed. Accordingly, there is an ongoing need to develop therapeutics to combat anthrax infection.